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Famotidine, one of the histamine H2-receptor antagonists (H2-blockers), contains a sulfamoylamidine group. The sulfamoylamidine group contains a residue which is structurally similar to the sulfonamide group. This group is known to have a carbonic anhydrase (CA) inhibitory action. In the present study, it was confirmed that famotidine inhibited CA activity in vitro whereas cimetidine and ranitidine which lack sulfonamide-like residues did not. Considering these characteristics of the H2-blockers, the effects of long-term administration of the H2-blockers on CA activity in gastric and duodenal mucosa were examined using the H2-blockers with or without CA-inhibiting action. After male adult Wistar rats were treated for 4 weeks with famotidine (1.6 mg/kg/day; F group) or cimetidine (32 mg/kg/day; C group), CA activity in the mucosa from the antrum, fundus or duodenum was measured on the 1st, 3rd, 7th, 14th or 21st day after the last administration. In spite of CA inhibitory action of famotidine in vitro, CA activity was not lower in the mucosal preparations from F group than in those from C group. Although CA activity in the duodenal mucosa was not significantly different from that in the control, CA activity in the gastric mucosa of both C and F groups clearly showed a decreasing tendency. These results suggest that long-term treatment with H2-blockers might diminish mucosal protection efficacy through mechanisms other than the direct CA inhibitory action.

Effect of long-term H2-blocker treatment on carbonic anhydrase in rat gastroduodenal mucosa.